Portal hypertension: state of the art

In the last decade, the knowledge of the pathogenesis of portal hypertension has increased dramatically. Indeed, apart from the well-known pathogenetic importance of structural factors, the role of vasoactive factors, which enhance the increase in intrahepatic resistance, has been highlighted. The two pathogenetic factors of portal hypertension are: the increase in portal outflow resistance and an increase in splanchnic blood flow, which worsens and maintains the increased pressure in the portal vein. The increase in portal inflow is part of the hyperdynamic circulatory syndrome, which is a haemodynamic characteristic of cirrhotic patients. In portal hypertensive patients, almost all the known vasoactive systems/substances are activated or increased and the most recent studies have stressed the importance of the endothelial factors, such as endothelins, nitric oxide and prostaglandins. Knowledge of the haemodynamic mechanisms allows a pathogenetic approach to the treatment of portal hypertension, particularly as far as medical therapy is concerned. The main categories of drugs used are: the vasoconstrictors (i.e., vasopressin, glypressin, somatostatin, non-selective beta-blockers), which act by decreasing portal inflow, and the vasodilators (i.e., nitroderivatives), which act mainly by decreasing intrahepatic portal resistance. Moreover, technological developments have introduced new tools for diagnosis, such as echo-colour-Doppler, and therapy, like variceal banding and transjugular intrahepatic porto-systemic shunt.